A role for the mitogen-activated protein kinase kinase kinase 1 in epithelial wound healing. Export

@article{citeulike:912481, abstract = {The mitogen-activated protein kinase kinase (MEK) kinase 1 (MEKK1) mediates activin B signals required for eyelid epithelium morphogenesis during mouse fetal development. The present study investigates the role of MEKK1 in epithelial wound healing, another activin-regulated biological process. In a skin wound model, injury markedly stimulates MEKK1 expression and activity, which are in turn required for the expression of genes involved in extracellular matrix (ECM) homeostasis. MEKK1 ablation or down-regulation by interfering RNA significantly delays skin wound closure and impairs activation of Jun NH2-terminal kinases, induction of plasminogen activator inhibitor (PAI)-1, and restoration of cell-cell junctions of the wounded epidermis. Conversely, expression of wild-type MEKK1 accelerates reepithelialization of full-thickness skin and corneal debridement wounds by mechanisms involving epithelial cell migration, a cell function that is partially abolished by neutralizing antibodies for PAI-1 and metalloproteinase III. Our data suggest that MEKK1 transmits wound signals, leading to the transcriptional activation of genes involved in ECM homeostasis, epithelial cell migration, and wound reepithelialization.}, address = {Department of Environmental Health and Center for Environmental Genetics, University of Cincinnati Medical Center, Cincinnati, OH 45267-0056, USA.}, author = {Deng, M. and Chen, W. L. and Takatori, A. and Peng, Z. and Zhang, L. and Mongan, M. and Parthasarathy, R. and Sartor, M. and Miller, M. and Yang, J. and Su, B. and Kao, W. W. and Xia, Y.}, citeulike-article-id = {912481}, citeulike-linkout-0 = {http://dx.doi.org/10.1091/mbc.E06-02-0102}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/16760432}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=16760432}, doi = {10.1091/mbc.E06-02-0102}, issn = {1059-1524}, journal = {Mol Biol Cell}, keywords = {cicatrizacin}, month = {August}, number = {8}, pages = {3446--3455}, posted-at = {2006-10-25 12:32:42}, priority = {1}, title = {A role for the mitogen-activated protein kinase kinase kinase 1 in epithelial wound healing.}, url = {http://dx.doi.org/10.1091/mbc.E06-02-0102}, volume = {17}, year = {2006} }

TY - JOUR ID - citeulike:912481 L3 - citeulike-article-id:912481 N2 - The mitogen-activated protein kinase kinase (MEK) kinase 1 (MEKK1) mediates activin B signals required for eyelid epithelium morphogenesis during mouse fetal development. The present study investigates the role of MEKK1 in epithelial wound healing, another activin-regulated biological process. In a skin wound model, injury markedly stimulates MEKK1 expression and activity, which are in turn required for the expression of genes involved in extracellular matrix (ECM) homeostasis. MEKK1 ablation or down-regulation by interfering RNA significantly delays skin wound closure and impairs activation of Jun NH2-terminal kinases, induction of plasminogen activator inhibitor (PAI)-1, and restoration of cell-cell junctions of the wounded epidermis. Conversely, expression of wild-type MEKK1 accelerates reepithelialization of full-thickness skin and corneal debridement wounds by mechanisms involving epithelial cell migration, a cell function that is partially abolished by neutralizing antibodies for PAI-1 and metalloproteinase III. Our data suggest that MEKK1 transmits wound signals, leading to the transcriptional activation of genes involved in ECM homeostasis, epithelial cell migration, and wound reepithelialization. IS - 8 JF - Mol Biol Cell SN - 1059-1524 AD - Department of Environmental Health and Center for Environmental Genetics, University of Cincinnati Medical Center, Cincinnati, OH 45267-0056, USA. EP - 3455 TI - A role for the mitogen-activated protein kinase kinase kinase 1 in epithelial wound healing. VL - 17 SP - 3446 KW - cicatrizacin AU - Deng, M AU - Chen, WL AU - Takatori, A AU - Peng, Z AU - Zhang, L AU - Mongan, M AU - Parthasarathy, R AU - Sartor, M AU - Miller, M AU - Yang, J AU - Su, B AU - Kao, WW AU - Xia, Y PY - 2006/08// UR - http://dx.doi.org/10.1091/mbc.E06-02-0102 ER -